{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T05:38:51Z","timestamp":1777354731921,"version":"3.51.4"},"reference-count":46,"publisher":"Oceanside Publications Inc.","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["allergy asthma proc"],"published-print":{"date-parts":[[2024,9,1]]},"abstract":"<jats:p>The immune system is divided into two major branches: innate and adaptive. The innate immune system is the body's first line of defense and rapidly responds in a nonspecific manner to various microorganisms, foreign materials, or injuries. Phagocytes, which include macrophages, monocytes,\n and neutrophils, are innate immune cells that can surround and kill microorganisms, ingest foreign material, and remove dead cells. They also indirectly boost both innate and adaptive immune responses through various activation signals. Phagocytic defects characteristically lead to fungal\n and bacterial infections of the respiratory tract, lymph nodes, skin, and other organ systems, and they are commonly associated with inflammatory bowel disease. This primer will review high-yield innate defects of phagocytic cells, including defects of respiratory (oxidative) burst, defects\n of neutrophil migration, cyclic and severe congenital neutropenias and associated disorders, and other phagocyte defect disorders.<\/jats:p>","DOI":"10.2500\/aap.2024.45.240049","type":"journal-article","created":{"date-parts":[[2024,9,19]],"date-time":"2024-09-19T04:31:59Z","timestamp":1726720319000},"page":"299-304","source":"Crossref","is-referenced-by-count":7,"title":["Immunodeficiency: Quantitative and qualitative phagocytic cell defects"],"prefix":"10.2500","volume":"45","author":[{"given":"David","family":"Mickey","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Juanita Valdes","family":"Camacho","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adil","family":"Khan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Kaufman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1355","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"e220","DOI":"10.1111\/ijlh.13265","article-title":"Prevalence of myeloperoxidase deficiency determined using an ADVIA 2120i","volume":"42","author":"Gleghorn","year":"2020","journal-title":"Int J Lab Hematol"},{"key":"B2","doi-asserted-by":"crossref","first-page":"97","DOI":"10.1172\/JCI3312","article-title":"A novel leukocyte adhesion deficiency caused by expressed but nonfunctional beta2 integrins Mac-1 and LFA-1","volume":"103","author":"Hogg","year":"1999","journal-title":"J Clin Invest"},{"key":"B3","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1016\/S0022-1759(99)00146-5","article-title":"Respiratory burst in human neutrophils","volume":"232","author":"Dahlgren","year":"1999","journal-title":"J Immunol Methods"},{"key":"B4","doi-asserted-by":"crossref","first-page":"155","DOI":"10.1097\/00005792-200005000-00003","article-title":"Chronic granulomatous disease. 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